Evidence map›Paper›PMID 41640232›Full record

ArticleJournal of the peripheral nervous system : JPNS2026

Serum Neurofilament Light Chain and Glial Fibrillary Acidic Protein as Biomarkers in Hereditary Transthyretin Amyloidosis Polyneuropathy.

Valentin Loser, Pascal Benkert, Alex Vicino, Nicolas Ghika, Pansy Lim Dubois Ferrière, Chantal Daigneault, Thierry Kuntzer, Aleksandra Maleska Maceski, Jens Kuhle, Marie Théaudin

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Article in Journal of the peripheral nervous system : JPNS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Valentin LoserNerve-Muscle Unit, Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.ORCID https://orcid.org/0000-0002-2609-6843
Pascal BenkertMultiple Sclerosis Centre and Research Centre for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland.
Alex VicinoNerve-Muscle Unit, Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.ORCID https://orcid.org/0000-0001-6420-8124
Nicolas GhikaNerve-Muscle Unit, Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Pansy Lim Dubois FerrièreNerve-Muscle Unit, Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Chantal DaigneaultNerve-Muscle Unit, Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Thierry KuntzerNerve-Muscle Unit, Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Aleksandra Maleska MaceskiMultiple Sclerosis Centre and Research Centre for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland.
Jens KuhleMultiple Sclerosis Centre and Research Centre for Clinical Neuroimmunology and Neuroscience (RC2NB), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Basel, Switzerland.
Marie ThéaudinNerve-Muscle Unit, Service of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsIn individuals with hereditary transthyretin amyloidosis (ATTRv) polyneuropathy, monitoring of disease progression and treatment response is crucial. The objective is to determine if serum neurofilament light chain (sNfL) and serum glial fibrillary acidic protein (sGFAP) are reliable biomarkers of ATTRv polyneuropathy.

methodsWe included 48 ATTRv individuals (38 symptomatic, 10 asymptomatic). Yearly assessments (over 4 years) included a full clinical examination with disease severity and functional scores, electrochemical skin conductance, nerve conduction studies, and measurement of sNfL and sGFAP levels. Using a reference database, sNfL and sGFAP were converted to Z-scores (zNfL and zGFAP).

resultsMedian zNfL was -0.50 in asymptomatic, 1.44 in converters, and 2.46 in symptomatic subjects. zNfL > 1.42 discriminated symptomatic from asymptomatic subjects (AUC 0.936), not zGFAP (AUC 0.588). zNfL, not zGFAP, correlated with most clinical and electrophysiological neuropathy severity scales. Two asymptomatic carriers became symptomatic during follow-up. In one of them, a significant rise in zNfL occurred 1 year before symptomatic transition.

interpretationIn ATTRv, zNfL correlates with neuropathy severity and symptomatic transition. A zNfL > 1.42 may discriminate symptomatic from asymptomatic subjects. zGFAP is not a reliable biomarker of polyneuropathy in ATTRv. Routine use of NfL should be based on deviation measure such as Z-score.

Indexed as

Amyloid Neuropathies, FamilialGlial Fibrillary Acidic ProteinNeurofilament ProteinsPolyneuropathiesAdultAgedBiomarkersDisease ProgressionFemaleHumansMaleMiddle AgedNerve Conduction StudiesSeverity of Illness IndexBiomarkersGFAP protein, humanGlial Fibrillary Acidic Proteinneurofilament protein LNeurofilament ProteinsamyloidosisATTRGFAPneurofilamentNfLZ‐score

Identifiers

PMID41640232
PMCPMC13285900

What Socratic holds

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.